Heart failure affects approximately three million Americans, and new cases of heart failure number about 400,000 each year. Congestive heart failure (CHF) is particularly insidious, affecting at least two million Americans, and is a syndrome characterized by left ventricular dysfunction, reduced exercise tolerance, impaired quality of life, and markedly shortened life expectancy. In patients suffering from CHF, decreased contractility of the left ventricle leads to reduced cardiac output with consequent systemic arterial and venous vasoconstriction. This vasoconstriction, which promotes the vicious cycle of further reductions of stroke volume followed by an increased elevation of vascular resistance, appears to be mediated, in part, by the renin-angiotensis system. The key component of this system, the potent vasoconstrictor angiotensin II, also has the effect of stimulating aldosterone secretion, possibly enhancing sympathetic drive and increasing vasopressin secretion. Cohn, J. N. et al., N. England J. Med. 325(5):303-310 (1991).
Drugs are sometimes employed to assist in treating problems associated with cardiac dilation. For example, digoxin increases the contractility of the cardiac muscle and thereby causes enhanced emptying of the dilated cardiac chambers. On the other hand, some drugs such as beta-blocking drugs decrease the contractility of the heart and therefore increase the likelihood of dilation. Other, pharmacological and/or biopharmaceutical treatments have been used previously. For example, angiotensin-converting enzyme (ACE) inhibitors, such as captopril and enalopril, have become standard therapy for patients with congestive heart failure. These drugs improve hemodynamic profile and exercise tolerance and reduce the incidence of morbidity and mortality in patients with congestive heart failure. However, despite these effects, the degree of clinical efficacy has been limited. Improvement in functional capacity and exercise time is small and mortality, although reduced, continues to be high. Moreover, many of these drugs have side effects which make them undesirable for long-term use.
Another approach has been to use a chronic hypersecretion of growth hormone (GH) in an attempt to induce a pattern of myocardial contraction that allows the cardiac muscle to function more economically. Timsit, J. et al., J. Clin. Invest. 86:507-515 (1990); Timsit, J. et al., Acta. Paediatr. Suppl. 383:32-34 (1992). The increase in the contractile performance was shown to be due to specific alterations in the properties of the contractile apparatus, including an increase in both maximal tension and myofibrillar sensitivity to calcium. Mayoux, E. et al., Circulation Research 72(1):57-64 (1993). Similarly, acute intravenous administration (infusion or bolus injection) of Insulin-like growth factor (IGF-I) produces increases in stroke volume and cardiac output in normal lambs. Gluckman et al., PCT WO 92/11865 (1992). It has also been suggested that improvement in cardiac performance for patients with congestive heart failure may be achieved by combining ACE inhibitors with a treatment regimen of GH and IGF-I. To date, however, none of the therapies discussed above have been approved for use in human patients.
Although a prominent symptom of CHF, cardiac dilation occurs as a result of many forms of cardiac disease. In some cases, such as post-myocardial infarction, the dilation may be localized to only a portion of the heart. In other cases, such as hypertrophic cardiomyopathy, there is typically increased resistance to filling of the left ventricle with concomitant dilation of the left atria. In dilated cardiomyopathy, the dilation is typically of the left ventricle with resultant decreased cardiac efficiency, and the continuing failure of the heart to adequately pump. With each type of cardiac dilation, there are associated problems ranging from arrhythmia which arise due to the stretch of myocardial cells, to leakage of the cardiac valves due to enlargement of the valvular annulus.
In addition to the treatments set forth above, devices to prevent or reduce cardiac dilation and thereby reduce the consequences of dilation are also know. For example, patches made from low porosity materials of the type used to repair cardiac ruptures and septal defects, such as Dacron.TM. have also been applied to support the cardiac wall where no penetrating lesion is present. This concept has been expanded to devices that attempt to constrain dilation. For example, U.S. Pat. No. 5,702,343--Alfernes, which is assigned to Acorn Medical, discloses a device applied to the epicardial surface of the heart for reinforcement of the cardiac wall during diastolic chamber filling to prevent or reduce cardiac dilation. The device includes a biomedical material applied to the epicardial surface that expands to a predetermined size to constrain cardiac expansion beyond a predetermined limit. The device may be a patch, or alternatively, a jacket with a predetermined size that surrounds the heart circumferentially. Similarly, U.S. Pat. No. 5,800,528--Lederman, et al. which is assigned to Abiomed R&D, Inc. discloses maintaining a passive girdle around a patient's heart and gradually reducing the size of the girdle to effect a constriction of the ventricle over time, thus preventing further dilation and attempting to reduce volume.
In addition to drugs and constraining structures, another method of treating CHF is by cardiac rhythm management devices such as dual chamber pacemakers. U.S. Pat. No. 5,800,471--Baumann, which is assigned to Cardiac Pacemakers, Inc. In the disclosed pacemaker, the pacing mode-AV delay is adjusted by sensing atrial and ventricular depolarization events to attempt to optimize hemodynamic performance. A similar dual chamber pacing system is disclosed n U.S. Pat. No. 5,749,906--Kieval et al., which is assigned to Medtronic, Inc. The dual pacing solution, although somewhat effective, has to date met with limited clinical success, largely due to the variability of the signals collected to determine the pacing mode.
Finally, treating CHF with invasive surgical remedies such as cardiomyoplasty has to date also led to little clinical gain. As explained in U.S. Pat. No. 5,738,626--Jarvik, cardiomyoplasty is a high mortality procedure with little clinical benefit (50% at two years) with limited hemodynamic benefit, and an even more radical approach--excision of a portion of the myocardium--is said to provide improved cardiac function although the mortality is still forty percent (40%) at one year. The Jarvik patent proposes a combination of excision followed by myoplasty. Others have suggested that the efficacy of myoplasty can be improved by the functional neuromuscular electrical stimulation of the transected skeletal muscle, e.g., U.S. Pat. No. 5,752,978--Chancellor.
Thus, there remains a long felt, yet to date unmet need to provide a therapeutic solution to minimize the deterioration of the heart associated with CHF.
Accordingly, it is an object of this invention to provide apparatus and methods whereby the heart is constrained from dilation.
It is another object of this invention to provide apparatus and methods that will assist physicians in collecting treatment data, as well as providing therapy.